Cirrhosis of the Liver and Liver Failure

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Cirrhosis of the Liver andLiver Failure

• Developed by
• Cheryl McConnell RN MSN

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Pathophysiology

• Slow, insidious, progressive, chronic
• Fibrous bands replace normal liver structure
• Cell degeneration occurs
• Liver attempts to regenerate cells but cells are
  abnormal and disorganized
• Causes abnormal blood and lymph flow
• Results in more fibrous tissue formation

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Normal Liver
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Incidence of Cirrhosis

• Tenth leading cause of death in US
• At least 25,000 deaths annually
• Higher death rates for men than women
• ? mortality in African Americans and Hispanics

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Types of Cirrhosis

• Laennecs (alcoholic)
• Postnecrotic
• Biliary
• Cardiac

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Laennecs Cirrhosis

• Most common type of cirrhosis
• Also called alcoholic or portal
• Alcohol causes inflammation to liver cells
• Leads to fatty deposits and hepatomegaly
• Scarring formed and liver cells destroyed
• Malnutrition and more alcohol accelerate the
  damage

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Postnecrotic Cirrhosis

• Caused by viral hepatitis or hepatotoxins
• Scar tissue destroys liver lobes
• Liver initially enlarges but then shrinks in size
• 10 30 of all cirrhoses

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Biliary Cirrhosis

• Caused by chronic biliary obstruction or stasis
  of bile, biliary inflammation, or hepatic
  fibrosis
• Excessive bile leads to liver cell destruction
  and formation of nodules in the lobes
• 5 10 of all cirrhoses

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Cardiac Cirrhosis

• Seen with right sided heart failure
• Liver is engorged with venous blood
• Becomes enlarged, edematous, and dark
• Venous congestion results in anoxia
• Cell necrosis results

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Diagnostic Data

• ? AST, ALT, LDH, Alk phos
• ? bilirubin, ammonia,
• ? coagulation studies
• Serum protein levels depend on disease
• ? with acute liver disease
• ? with chronic liver disease

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More Diagnostics

• Abdominal x-ray
• Upper GI series
• Angiography
• Abdominal CT
• EGD
• Liver biopsy
• Nuclear scan

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Signs and Symptoms

• Neurological
• Asterixis Paraesthesias
• LOC Sensory disturbances
• Behavorial changes Cognitive changes
• Skin
• Spider angiomas Palmar erythma
• Jaundice Pruitis
• ? hair production caput medusa
• ? pigmentation Bruising
• White Nails

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Caput Medusae
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Spider Angiomas
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Palmar Erythema
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More Signs and Symptoms

• GI
• Abdominal pain Anorexia
• Ascites Diarrhea
• Clay colored stools Fetor hepaticus
• Gastritis GI bleeding
• N/V Varices
• Malnutrition

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White Nails
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More Signs and Symptoms

• Cardiovascular
• Dysrhythmias Portal hypertension
• Collateral circulation Fatigue
• Peripheral edema
• Endocrine
• Gynecomastia Amenorrhea
• ? aldosterone, ADH, estrogens, glucocorticoids

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More Signs and Symptoms

• Respiratory
• Dyspnea Hypoxia
• Blood
• Anemia DIC
• Thrombocytopenia ? WBCs
• Hypokalemia Hypocalcemia
• Hypo/Hypernatremia
• Hypomagnesia

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More Signs and Symptoms

• Immune
• ? Susceptibility to infections Leukopenia
• Renal
• ? Urinary output

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Complications

• Portal hypertension
• Ascites
• Varices
• Coagulation defects
• Jaundice
• PSE (portal systemic encephalopathy)
• Hepatorenal syndrome

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Portal Hypertension

• Increased pressure within the portal vein
• Results in obstruction of blood flow through the
  portal vein
• Blood tries to find new ways around obstructed
  area collateral circulation
• Causes venous distention in entire GI tract

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Ascites

• Accumulation of plasma in the peritoneal cavity
• Caused by increased pressure forcing fluid out of
  intravascular space into cavity
• Plasma contains albumin so circulating proteins
  decreased
• ? serum osmotic pressure
• Intravascular fluid depletion stimulates kidney
  to conserve sodium and water ? hydrostatic
  pressure and creates more ascites

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Ascites
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Varices

• Occur anywhere in the GI tract especially
• Esophageal Hemorrhoids
• Bleeding esphageal varices
• Caused by thin walled veins that are irritated,
  distended and eventually rupture
• Chemical irritants Mechanical trauma
• Esophagus pressure
• Prone to hemorrhage medical emergency

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Esophageal Varices
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Coagulation Defects

• Susceptible to bleeding
• Bruises easily
• Does not clot
• Esophageal varices bleeding

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Jaundice

• Due to hepatocellular destruction or hepatic
  obstruction
• Hepatocellular cannot metabolize bilirubin so
  it builds up
• Obstruction clogs bile ducts so excretion is
  not possible

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Jaundice
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PSE

• Also known as hepatic coma
• Seen in end stage hepatic failure
• Can be insidious or rapid onset depending on the
  severity of liver disease
• Caused by impaired ammonia metabolism

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PSE Continued

• Usually protein breaks down into ammonia in GI
  tract, then ammonia into urea --- excreted by the
  kidneys
• Liver cannot convert ammonia into urea
• Results in ? serum ammonia levels
• Toxic to the central nervous system

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PSE Continued

• Other factors that add to PSE
• High protein diet Infection
• Hypovolemia Constipation
• GI bleeding Medications

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Stages of PSE

• 1 - Prodomal very subtle changes
• Personality/behavior changes
• Impaired thinking/concentration
• Emotional highs and lows
• Fatigue, drowsiness
• Slurred or slow speech
• Sleep pattern disturbance

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Stages of PSE

• 2 Impending
• Continued mental deterioration
• Confusion
• Disoriented
• Asterixis

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Stages of PSE

• 3 Stuporuous
• Marked mental confusion
• Drowsy but arousable
• Abnormal EEG
• Muscle twitching
• Hyperreflexia
• Continued asterixis

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Stages of PSE

• 4 Comatose (85 mortality rate)
• Unresponsive
• Responds to painful stimuli only
• No asterixis
• Positive Babinskis sign
• Muscle rigidity
• Fetor hepaticus
• Seizures

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Hepatorenal Syndrome

• A primary cause of death with hepatic
  failure/cirrhosis
• Kidneys cannot excrete ammonia and bilirubin
• Results in acute tubular necrosis
• Signs/symptoms
• Sudden ? urinary output
• ? BUN, Cr, urine osmolarity ? Urine Na

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Treatment

• Diet
• ? Sodium (lt 2 grams)
• ?Carbohydrate, moderate fats
• ? Protein
• Unless PSE present then ? protein
• Fluid restriction (total of 1500cc/day)
• Vitamin supplements

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Treatment Continued

• Medications
• Diuretics
• Electrolyte replacement
• Antacids
• Must be low sodium Riopan
• Lactulose
• Facilitates evaculation of ammonia
• Neomycin
• Eliminates intestinal flora ? protein breakdown
• Levadopa
• For PSE repairs damaged neurotransmitters

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More Treatments

• Ascites control
• Paracentesis
• Shunts
• Le Veen Shunt - drains ascites fluid into
  superior vena cava
• Denver Shunt subcutaneous pump that is manually
  compressed
• Post op care same as with any abdominal
  surgery, watch for fluid volume overload and
  bleeding disorders, measure abdominal girth every
  shift

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Le Veen Shunt
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More Treatments

• Hemorrhage from varices
• Esophagogastric balloon tamponade
• Sengstaken-Blakemore tube balloon inflates in
  esophagus and puts pressure on varices
• Blood transfusions
• Medications
• Beta blockers to decrease HR and BP
• Pitressin (vasopressin) IV or into superior
  mesenteric artery (via endoscopy)
• Sclerotherapy
• Sclerosing agents injected into varices during
  EGD
• Transjugular intrahepatic portal systemic shunt
  (TIPS)
• Shunt between portal and hepatic vein to ?
  pressure ? bleeding
• Other portal system shunts poor prognosis

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Sclerosing Procedure
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Blakemore Tube
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Another Blakemore Tube
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More Treatments

• PSE
• Low protein diet
• May need TPN
• Control GI bleeding
• Medications
• Neuro checks
• Look for signs and symptoms of the stages of PSE

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Home Care

• Diet
• ? calories, vitamins, protein (unless PSE)
• ? sodium
• Medications
• Diurectics
• Antacids, H2-receptor antagonists
• No OTC medications
• No alcohol consumption
• ? activity rest periods
• Home care equipment

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Evaluation Outcomes

• Patient will
• ? in ascites
• Electrolytes WNL
• B/P WNL
• No bleeding or complications from bleeding
• PSE managed immediatley
• Optimal quality of life

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EVOLUTIE
Ciroza compensata ? ciroza decompensata vascular
si parenchimatos Rezerva functionala
Clasificarea Child Pugh
Parametru Albumina serica Ascita Encefalopatia Bil
irubina Indicele Quick

• 1 pct.
• gt3,5
• Abs
• Abs
• lt 2
• gt 70

2 pct. 2,8-3,5 Moderata Grd. I, II 2-3 40-70

• 3 pct.
• lt 2,8
• Mare
• Grd. III, IV
• gt 3
• lt 40

A 5-6 pct., B 7-9 pct., C 10-15 pct.
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